Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

c-Met Mouse anti-Human, Clone: 85503, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA523760

Catalog No. PIMA523760


Add to cart

Description

Description

In sandwich ELISAs, no cross-reactivity with recombit human (rh) EGFR or rhIGF-1 R is observed. Reconstitute at 0.5 mg/mL in sterile PBS.

The c-Met oncogene was originally isolated from a chemical carcinogen-treated human osteogenic sarcoma cell line by transfection analysis in NIH/3T3 cells. The Met proto-oncogene product was identified as a trans-membrane receptor-like protein with tyrosine kinase activity that is expressed in many tissues. The c-Met gene product has been identified as the cell surface receptor for hepatocyte growth factor, a plasminogen-like protein thought to be a humoral mediator of liver regeneration.
Specifications

Specifications

c-Met
Monoclonal
0.5 mg/mL
PBS with 5% trehalose and No Preservative
P08581
EC 2.7.10.1, HGF receptor, HGF-SF receptor, Hepatocyte growth factor receptor precursor, Met proto- oncogene tyrosine kinase, c-met, kinase EC 2.7.10.1, HGF receptor, HGF-SF receptor, Hepatocyte growth factor receptor precursor, Met proto- oncogene tyros
Mouse
IgG1
500 μg
-20° C, Avoid Freeze/Thaw Cycles
Primary
4233
ELISA
85503
Unconjugated
MET
Lyophilized
MET
Mouse myeloma cell line NS0-derived recombit human HGF R/c-MET Glu25-Thr932
Protein A/G
RUO
Antibody
Monoclonal
Human
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit